Presentation

A mitochondrial gate to neuronal plasticity and neurodegeneration.

Finely tuned mitochondrial functions, from energy supply to cell homeostasis, are vital for highly specialized and energy-demanding cells, like neurons. A precise dynamics of mitochondrial fusion and fission events underlies their quality control and adaptability to cellular needs. As an illustration, pathologies directly associated to mutations in key fusion proteins, like Type 1 Dominant Optic Atrophy (OPA1 mutation), are mainly neurodegenerative. Reciprocally, progressive neurodegenerative diseases such as Alzheimer’s are linked not only to impairments of mitochondrial functions (energy, oxidative stress) but also to impairments of mitochondrial dynamics and turn-over.

Mainly centered on in vitro and in vivo DOA models, our projects aim at deciphering, and in fine modeling, the mechanisms of mitochondrial impact on neuronal homeostasis and synaptic plasticity. Spanning from adult neurogenesis to axonal degeneration, we also want to understand the impact of mitochondrial morphological and functional plasticity on experience-dependent neuronal plasticity and complex brain functions such as animal cognition.